Melnik B, Plewig G
Hautklinik, Heinrich-Heine Universität Düsseldorf.
Hautarzt. 1991 Apr;42(4):211-4.
The concept proposed for the pathogenesis and prevention of atopy [Hautarzt (1989) 40:685-692] is refined by further insights into the immunoregulatory role of E-prostaglandins. It is demonstrated that in vitro IgE synthesis of peripheral blood mononuclear cell cultures of patients with atopic dermatitis is suppressed by the addition of PGE1 or PGE2. The enhanced IgE production in atopy is explained by insufficient PGE-mediated down-regulation of interleukin-4-induced IgE synthesis.
通过对E-前列腺素免疫调节作用的进一步深入了解，完善了先前提出的特应性发病机制及预防的概念[《皮肤病学文献》（1989年）40:685 - 692]。研究表明，添加PGE1或PGE2可抑制特应性皮炎患者外周血单核细胞培养物的体外IgE合成。特应性中IgE产生增加是由于PGE介导的白细胞介素-4诱导的IgE合成下调不足所致。
